Abstract

The syndrome of hyperventilation is observed frequently and is well recognized. Its pathogenesis, however, is not understood as well. It was the purpose of this study to elucidate the mechanism of the clinical syndrome with observations of respiratory function, biochemical changes, and electroencephalographic alterations during voluntary hyperventilation of one hour. Observations were made on eight normal students.

Voluntary hyperventilation decreased arterial carbon dioxide tensions (PCO2) to 15 to 25 mm. Hg within five minutes. The minute ventilation then decreased spontaneously and brief periods of apnea were observed. During the remainder of the study, the markedly hypocapnic levels were maintained with